Hypoxemic reperfusion after 120 mins of intestinal ischemia attenuates the histopathologic and inflammatory response

Objective. It has been suggested that reactive oxygen species play a pivotal role in the initial organ-tissue injury during reperfusion, eliciting inflammatory reaction and multiple organ failure. It was investigated if hypoxemic reperfusion attenuates tissue injury and inflammatory response. Design: Randomized animal study. Setting. Medical school laboratory. Subjects. Twenty-five male pigs weighing 25-28 kg. Interventions. Pigs were subjected to 120 mins of intestinal ischemia by clamping the superior mesenteric artery. Upon declamping, the animals were randomly assigned to receive either hypoxemic reperfusion (HR group, n = 9) reperfused with a PaO2 = 30-35 or normoxemic reperfusion (control group, n = 16) reperfused with a PaO2 = 100 mm Hg for 120 mins. Fluids without inotropes were given to combat circulatory shock during reperfusion. Measurements and Main Results. Portal blood and intestinal and lung biopsies were collected at baseline, end of ischemia, and end of reperfusion. Histopathologic changes were scored, and interleukin-1 beta, qualitative Limulus amebocyte, lysate test, and PaO2/F10(2) were measured. Eight of 16 animals of the control group and seven of nine of the HR group survived (p =. 22). At the end of reperfusion, the intestinal (p =.004) and lung (p =.028) pathologic scores were lower in the HR group compared with controls. The only significant difference in concentration of interleukin-1 beta in the portal blood between the two animal groups occurred 120 mins after reperfusion (p =.006). The number of HR animals with a positive Limulus test was significantly smaller compared with controls at 60 (p =.041) and 120 (p =.07) mins of reperfusion. During the period of ischemia, the Pao(2)/F10(2) decreased similarly in the control and HR group, whereas after 120 mins of reperfusion the rate was significantly higher in the HR group. Conclusions. Hypoxemic reperfusion represents an intervention that may attenuate the triggering of multifactorial cascade and organ tissue injury.